ライフサイエンスコーパス: bile salt

1 nd phospholipid molecules to be excreted per bile salt.

2 zed using a fluorescently labeled conjugated bile salt.

3 ce to pepsin and pancreatin and tolerance to bile salts.

4 ociated with increased circulating levels of bile salts.

5 R upregulated leuO expression in response to bile salts.

6 e type III secretion system 2 in response to bile salts.

7 regulated carRS transcription in response to bile salts.

8 rC complex activates VtrB in the presence of bile salts.

9 ention of toxic bile constituents, including bile salts.

10 suggested residual enterohepatic cycling of bile salts.

11 using hydropropyl-cyclodextrins (HP-CDs) and bile salts.

12 tance of enteric bacteria to acetic acid and bile salts.

13 urocholate (STC) belongs to a major class of bile salts.

14 biliary tree from the detergent activity of bile salts.

15 mal plasma levels ( approximately 10 muM) of bile salts.

16 HVs on PPIs were associated with changes in bile salts.

17 a key role in the intracellular transport of bile salts.

18 ts and aggregative growth in the presence of bile salts.

19 flexneri strain 2457T following exposure to bile salts.

20 yo-EM structures of MNV-1 in the presence of bile salts (~3 angstrom) and the receptor CD300lf (~8 an

21 M, and its activity requires the presence of bile salts, a class of physiological anionic detergents.

22 eres with basolateral uptake of unconjugated bile salts, a process mediated by organic anion-transpor

23 together with kinetic analysis, reveals that bile salts act as partial non-competitive inhibitors of

24 Bile salts act as steroidal detergents in the gut, and c

25 In rat liver, excess levels of bile salts activate a GAPDH-mediated transnitrosylation

26 s, cucurbit[n]urils, DNA, serum albumins and bile salt aggregates are presented that describe the typ

27 e complex thermodynamic interactions between bile salts alone or with phospholipids, i.e. mixed micel

28 A co-crystal structure of VtrA/VtrC with bile salt, along with biophysical and mutational analysi

29 We recently reported that CamSA, a bile salt analog, inhibits C. difficile spore germinatio

30 The kinetics of passage of a model bile salt and complete porcine bile across a dialysis me

31 strategies to accelerate renal excretion of bile salt and other toxins should be beneficial for pati

32 but not of wcaG, decreased susceptibility to bile salts and abrogated invasion of intestinal cells.

33 onstrates that the hydrophobic chamber binds bile salts and activates the virulence network.

34 nsive to various environmental cues, such as bile salts and alkaline pH, but how these factors influe

35 Trimethylamine, cadaverine, bile salts and amino acids could play a role in the mech

36 study, we define mechanisms of resistance to bile salts and build on previous research highlighting i

37 FRAP) analysis demonstrated that exposure to bile salts and Ca(2+) together decreases the recovery ra

38 ry transporters, which expose hepatocytes to bile salts and cause chronic inflammation that develops

39 n sugar composition, promoting resistance to bile salts and cell wall integrity.

40 ining envZP41L also became more resistant to bile salts and colicin V and grew 50% slower in vitro in

41 an important physiological route to recycle bile salts and ensure intestinal absorption of dietary l

42 Serum levels of bile salts and FGF19 were assessed.

43 flexneri 2457T biofilms determined that both bile salts and glucose were required for formation, disp

44 permeability barrier and hypersensitivity to bile salts and sodium dodecyl sulfate.

45 logical response to CAC, brine shrimp rinse, bile salt, and amino acid cues using the electro-olfacto

46 esolution cryo-EM structures of apo MNV, MNV/bile salt, and MNV/bile salt/receptor.

47 genous organic anions, including biliverdin, bile salts, and BSP, were predominantly excreted by way

48 increased intrahepatic and biliary levels of bile salts, and deficiency in repression of CYP7A1 (at t

49 erature could influence micellar behavior of bile salts, and in turn whether this affected the biolog

50 defense against detergents such as EDTA and bile salts, and resistance to antimicrobial peptides pol

51 und two key microbial pathways for degrading bile salts, and the impact of bile acid composition in t

52 Therefore, bile salts appear to be having several effects on MNV.

53 Furthermore, our work confirms that bile salts are important physiological signals to activa

54 Bile salts are secreted into the gastrointestinal tract

55 mainly from the reduced level of enzymes and bile salts, as well as the higher gastric pH in the infa

56 f the Lab4 probiotic consortium to hydrolyse bile salts, assimilate cholesterol and regulate choleste

57 , reduction of hepatic cholesterol and serum bile salts, bilirubin, and transaminase levels.

58 o the sugarcane fibre potentially indicating bile salt binding activity.

59 in the binding process, the pH-dependence of bile salt binding and internal dynamics in hI-BABP was i

60 The difference in bile salt (BS) composition between rodents and humans is

61 a-D-glucan (betaG) and arabinoxylan (AX) and bile salt (BS) or diluted porcine bile, were identified

62 ) and high-hydrostatic-pressure (HHP) on the bile salt (BS)-binding ability of dry beans, and how thi

63 tually leads to cholestasis, and this causes bile salt (BS)-mediated toxic injury of the "upstream" l

64 g of BDL mice was performed with fluorescent bile salts (BS) and non-BS organic anion analogues.

65 mprovement, we studied the biliary output of bile salts (BS) and the functional expression of the can

66 dylcholine aqueous dispersions stabilized by bile salts (BS) under simulated intestinal conditions (p

67 osed of soybean phosphatidylcholine with the bile salts (BSs) cholate (Ch), glycocholate (GC), chenod

68 langiocytes from the proapoptotic effects of bile salts by maintaining them deprotonated.

69 Bile salts cause a 90 degrees rotation and collapse of t

70 We then show that a set of bile salts cause dimerization of the transmembrane trans

71 Surprisingly, bile salts cause the rotation and contraction of the P d

72 Here, we show that bile salts cause widespread protein unfolding and aggreg

73 re, using NMR and DSF, it was shown that the bile salts cholate and chenodeoxycholate interact with p

74 cretion whereas biliary bile salt output and bile salt composition remains unchanged.

75 eys tolerate cholestasis by altering hepatic bile salt composition, while maintaining normal plasma b

76 protect periportal hepatocytes from harmful bile salt concentrations.

77 sion site, conferring full resistance to the bile salt deoxycholate, improving the efficiency of cell

78 growth and tolerance during stress from the bile salt deoxycholate.

79 We then found bile salt-dependent effects of these cysteine mutations

80 e does not affect virulence, Ca(2+) enhances bile salt-dependent virulence activation for V. cholerae

81 for formation, dispersion was dependent upon bile salts depletion, and recovered bacteria displayed i

82 minated hydrophobic tail was combined with a bile salt derivative, divinyl benzene (DVB), and a photo

83 Strong and selective binding of bile salt derivatives was obtained, depending on the cro

84 rthermore, it plays a key role in converting bile salt-derived taurine into H(2)S in the disease-asso

85 Surprisingly, bile salt destabilization of ToxRp enhanced the interact

86 challenged with a high fat/high cholesterol/bile salt diet, T39(-/-) mice or mice with hepatocyte-sp

87 SEC length fractionation can be achieved for bile salt dispersed SWCNTs by using porous silica-based

88 shed in faeces and stripped of membranes by bile salts during passage through the bile ducts to the

89 oups, nutrient infusion elicited substantial bile salt elevations (P < 0.001), peaking at 90 minutes,

90 Recently, we demonstrated that bile salts enhance cell attachment to the target cell an

91 Recent studies demonstrated that bile salts enhance the intrinsic P domain/receptor affin

92 h retrieval of the canalicular transporters, bile salt export pump (Abcb11) and multidrug resistance-

93 rum alpha-fetoprotein and undetectable liver bile salt export pump (ABCB11) expression.

94 the two main canalicular bile transporters, bile salt export pump (BSEP) and multidrug resistance pr

95 age induces a Fyn-dependent retrieval of the bile salt export pump (Bsep) and multidrug resistance-as

96 l intrahepatic cholestasis-1 (FIC1), 18 with bile salt export pump (BSEP) disease, and 4 others with

97 tasis type 2 patients and how they relate to bile salt export pump (BSEP) expression and its (re)targ

98 The liver-specific bile salt export pump (BSEP) is crucial for bile acid-de

99 Bile salt export pump (BSEP) is responsible for biliary

100 ced cholestasis due to the inhibition of the bile salt export pump (BSEP) is well investigated, only

101 As a canalicular bile acid effluxer, the bile salt export pump (BSEP) plays a vital role in maint

102 esistance-associated protein 2 (MRP2) and of bile salt export pump (BSEP) variants and mutants.

103 encies in the gene ABCB11, which encodes the bile salt export pump (BSEP), a liver-specific adenosine

104 expression; small heterodimer partner (SHP), bile salt export pump (BSEP), and increased Cyp7A1.

105 reactive metabolite formation, inhibition of bile salt export pump (BSEP), and mitochondrial dysfunct

106 In vitro assays to assess inhibition of the bile salt export pump (BSEP), mitotoxicity, reactive met

107 is a result of mutations in ABCB11 encoding bile salt export pump (BSEP), the canalicular bile salt

108 lysis showed that Sumo1 was recruited to the bile salt export pump (BSEP), the small heterodimer part

109 levels, small heterodimer partner (SHP), and bile salt export pump (BSEP).

110 r (FXR), small heterodimer partner (SHP) and bile salt export pump (BSEP).

111 e [organic solute transporter alpha/beta and bile salt export pump (BSEP)] promoter reporter activity

112 ultidrug resistance 3) rs2302387 and ABCB11 [bile salt export pump (BSEP)] rs4668115 reduce transport

113 The bile salt export pump (BSEP/ABCB11) transports bile salt

114 sed the hyperosmolarity-induced retrieval of bile salt export pump from the canalicular membrane.

115 ile salt export pump (BSEP), the canalicular bile salt export pump of hepatocyte.

116 from MYO5B(P663L) piglets had alterations in bile salt export pump, a transporter that facilitates bi

117 holestasis, namely ABCB11, which encodes the bile salt export pump, and ABCB4, which encodes hepatoca

118 in HE-iPSCs, resulting in the expression of bile salt export pump.

119 1 levels, hepatic HAX-1 deficiency increases bile salt exporter protein levels, thereby promoting ent

120 lability by forming insoluble complexes with bile salts/fatty acids, inhibiting micelle formation.

121 /-)(low) mice, were sensitive to hydrophobic bile salt feeding (0.3% glycochenodeoxycholate); they ra

122 10a1) with Myrcludex B, is expected to limit bile salt flux through the liver and thereby to decrease

123 le salt export pump (BSEP/ABCB11) transports bile salts from hepatocytes into bile canaliculi.

124 dent bile acid transporter (ASBT) transports bile salts from the lumen of the gastrointestinal (GI) t

125 ocess as the major transporter of conjugated bile salts from the plasma compartment into the hepatocy

126 . difficile is regulated by the detection of bile salt germinants and amino acid cogerminants by pseu

127 We found that the toxic bile salt glycochenodeoxycholate (GCDC) rapidly fragment

128 as previously shown that the presence of the bile salts glycocholate and taurocholate in the small in

129 rs were severely cholestatic, with levels of bile salts >1 mM, but no evidence of necrosis, fibrosis,

130 he capacity of MdtM to catalyse electrogenic bile salt/H(+) antiport.

131 explanation for the antimicrobial effects of bile salts, help explain the beneficial effects of bile

132 out the ability to secrete bile, we examined bile salt homeostasis in larval and adult lampreys.

133 rotein nitrosylation (via dithiothreitol) on bile salt homeostasis in male Wistar rats placed on a ch

134 e observed within the physiological range of bile salts; however, growth was inhibited at higher conc

135 lly reducing the genus Lactobacillus and its bile salt hydrolase (BSH) activity leading to the accumu

136 through deconjugation of bile salts through bile salt hydrolase (BSH) enzymatic activity, which is p

137 Using this approach we show that bacterial bile salt hydrolase (BSH) mediates a microbe-host dialog

138 The gut bacterial bile salt hydrolase (BSH) plays a critical role in host

139 lpha-hydroxylase mRNA expression, implicates bile salt hydrolase activity as a potential mechanism of

140 Faecal bile salt hydrolase activity was measured using a precip

141 Bile salt hydrolase activity was reduced in women with l

142 These demonstrate high bile salt hydrolase activity, which deconjugates bile ac

143 was reduced in pregnancy because of elevated bile salt hydrolase-producing Bacteroidetes.

144 f the gut through the activity of the enzyme bile salt hydrolase.

145 asmic function-sigma factors, a urease and a bile salt hydrolase.

146 inantly suppressing microbes associated with bile-salt hydrolase (BSH) activity.

147 conjugated bile acids-generated by bacterial bile salt hydrolases (BSH)-correlated with faster transi

148 Gut microbial enzymes, bile salt hydrolases (BSHs) are the gateway enzymes for

149 g for genes encoding glyosyltransferases and bile salt hydrolases.

150 of alterations in bile salt output, biliary bile salt hydrophobicity, or increased activity of dedic

151 highly acidic environment in the stomach and bile salt in the intestine.

152 the predominant bile salt, whereas the major bile salts in adult liver were sulfated C27 bile alcohol

153 lt synthesis, indicating that elevated serum bile salts in Fut2(-/-)(high) mice were not explained by

154 Total bile salts in plasma were extremely elevated (up to 1,50

155 Importantly, the presence of secondary bile salts in the circulation suggested residual enteroh

156 Resistance to high concentrations of bile salts in the human intestinal tract is vital for th

157 le of gastric treatments and the presence of bile salts in the release and bioaccessibility of encaps

158 -Gln-Trp, and Leu-Gln-Lys-Trp, and different bile salts in the submicellar or micellar state was inve

159 ivers reflecting increased concentrations of bile salts in these conditions.

160 y include elevated biomarkers of aspiration (bile salts) in bronchoalveolar lavage fluid (BALF).

161 owed by a 2 h incubation with pancreatin and bile salts including a cellulose dialysis tubing (molecu

162 It has been shown that a set of bile salts, including taurocholate, serve as host signal

163 In an in vitro setting, we demonstrate that bile salts increase SPI-6 antibacterial activity and tha

164 ide new insights into the mechanism by which bile salts induce V. cholerae virulence but also suggest

165 talized H69 human cholangiocytes to not only bile salt-induced apoptosis (BSIA) but also etoposide-in

166 s revealed that disruption of icsA abolished bile salt-induced biofilm formation.

167 drolysis of egg white proteins and abrogated bile salt-induced precipitation of LYS in the duodenal m

168 t exhibits anti-aggregation activity against bile salt-induced protein aggregation.

169 (cspE or STM14_0732) is up-regulated during bile salt-induced stress and that an S. Typhimurium stra

170 gical levels of Ca(2+) may result in altered bile salt-induced TcpP protein movement and activity, ul

171 that Ca(2+) enhances virulence by promoting bile salt-induced TcpP-TcpP interaction.

172 that exposure of esophageal cells to acidic bile salts induces phosphorylation of the p47(phox) subu

173 Bile salts inhibit their own production by inducing the

174 As drugs and bile salts interact, increasing the absorption of lipoph

175 BALF was assessed for pepsin, bile salts, interleukin-8 and neutrophils.

176 Active secretion of bile salts into the canalicular lumen drives bile format

177 ter is the main import system for conjugated bile salts into the liver but also indicates that auxili

178 of weak physiological allosteric inhibitors (bile salts) into potent competitive Autotaxin inhibitors

179 The enterohepatic circulation of bile salts is an important physiological route to recycl

180 Thus micellar breakdown of bile salts is essential for their entry into the systemi

181 d remedy containing onion, garlic, wine, and bile salts, known as 'Bald's eyesalve', and showed it ha

182 terestingly, extended periods of exposure to bile salts led to biofilm formation, a conserved phenoty

183 Half of the Fut2(-/-) mice showed serum bile salt levels 40 times higher than wt (Fut2(-/-)(high

184 tes within just 4 h, with increasing primary bile salt levels in vitro and using ex vivo microbiota s

185 composition, while maintaining normal plasma bile salt levels predominantly through renal excretion o

186 ensal bacteria modulate primary to secondary bile salt levels to control germination.

187 The mechanism by which bile salts limit bacterial growth is still largely unkno

188 sing exposure of the canalicular membrane to bile salts linking to increased biliary cholesterol secr

189 During increased portal bile salt load this mechanism may adjust bile salt uptak

190 ile flow, biliary bile salt secretion, fecal bile salt loss, and expression of major hepatocellular b

191 altered intestinal permeability; disordered bile salt metabolism (in 10-20% of cases with diarrhoea)

192 clear hormone receptors in the regulation of bile salt metabolism, which has led to novel therapies u

193 released products (i.e. contained within the bile salt micellar phase).

194 adsorption site for pyrene and quercetin in bile salt micelles is more hydrophobic than that for SDS

195 xenosterols to high-density lipoprotein and bile salt micelles, respectively.

196 id quercetin we studied its interaction with bile salt micelles.

197 loop-that are essential for accessing SM in bile salt micelles.

198 id skeleton, and the acidic function of some bile salts, might promote the interaction with the pepti

199 products are very rapidly solubilized in the bile salt mixed micelles with no fractionation according

200 alts, help explain the beneficial effects of bile salt mixtures, and suggest that we have identified

201 cyte integrity in the presence of millimolar bile salt monomers is dependent on (1) pH, (2) adequate

202 exposed to millimolar levels of hydrophobic bile salt monomers.

203 samples were determined, and the effects of bile salts on fu were investigated in vitro.

204 together, these data suggest a model whereby bile salts or other detergents destabilize ToxR, increas

205 by catalysing secondary active transport of bile salts out of the cell cytoplasm.

206 l and phospholipid excretion whereas biliary bile salt output and bile salt composition remains uncha

207 tion, which is independent of alterations in bile salt output, biliary bile salt hydrophobicity, or i

208 d may act as a gatekeeper to prevent hepatic bile salt overload.

209 olera and for V. cholerae resistance against bile salts, perhaps due to environmental regulation of A

210 rough the GIT due to accumulation of anionic bile salts, phospholipids, and free fatty acids at their

211 Strategies that alter bile salt pool composition might be developed for the pr

212 iet (0.1%) resulted in a completely restored bile salt pool in Hrn mice, with 50% +/- 9% TDC and 42%

213 The altered bile salt pool stimulated robust secretion of cholestero

214 Alterations of the bile salt pool were mediated by increased expression of

215 Hydrophilicity of the bile salt pool, controlled by FXR and FGF15/19, is an im

216 cholate in bile, inducing a more hydrophilic bile salt pool.

217 in the composition and hydrophobicity of the bile salt pool.

218 Bile salts produced by the liver and secreted into the i

219 nalling and select steroids, notably natural bile salts, provides a molecular basis for the emerging

220 s CYP27A1 and CYP3A11 as well as canalicular bile salt pump ABCB11.

221 tructures of apo MNV, MNV/bile salt, and MNV/bile salt/receptor.

222 anced Claudin-2 expression in colon and that bile salt receptors VDR and Takeda G-protein coupled rec

223 major facilitator superfamily, functions in bile salt resistance in E. coli by catalysing secondary

224 d lipopolysaccharide O-antigen synthesis for bile salt resistance.

225 ation of ileal farnesoid X receptor (FXR) by bile salts results in transcriptional induction of FGF19

226 normal serum liver tests, bile flow, biliary bile salt secretion, fecal bile salt loss, and expressio

227 CU patients had significantly higher fasting bile salt serum levels compared with controls, whereas F

228 Bile salts shift the structural equilibrium of the P dom

229 In addition, bile salts show potent antimicrobial activity in part by

230 Dissecting individual roles of bile salts showed that deoxycholate is a robust biofilm

231 ed as a biofilm has coopted the host-derived bile salt signal to detach from the biofilm and go on to

232 Bile salt synthesis and intestinal bile salt signaling were not affected, as evidenced by n

233 Myrcludex B blocked NTCP transport of bile salts; small hairpin RNA-mediated knockdown of NTCP

234 lica-based beads as the stationary phase and bile salt solution as the mobile phase.

235 In the presence of bile salts, some released peptide monomers were bound to

236 cspE) displays dose-dependent sensitivity to bile salts, specifically to deoxycholate.

237 On the other hand, bile salts stimulate hepatic synthesis of nitric oxide.

238 ary cholesterol mass secretion under maximal bile salt-stimulated conditions is fully dependent on AB

239 lk composition and structure by inactivating bile salt-stimulated lipase (BSSL) and partially denatur

240 e heat-denaturated proteins, lactoferrin and bile salt-stimulated lipase, presented different kinetic

241 d revealed the involvement of WxL operons in bile salt stress and endocarditis pathogenesis.

242 hat an ompU deletion mutant was sensitive to bile salt stress but resistant to polymyxin B stress, in

243 genes, ompD, ompF, and ompC, were higher in bile salts-stressed DeltacspE and correlated with higher

244 c antimicrobial peptide polymyxin as well as bile salts, suggesting a role in outer membrane integrit

245 is accomplished by exchanging strong binding bile salt surfactant coating with DNA in methanol/water

246 Furthermore, bile salt survival assays and animal models using a muta

247 Hrn mice have strongly impaired bile salt synthesis and (re)hydroxylation capacity and a

248 Bile salt synthesis and intestinal bile salt signaling w

249 echanisms may shed light on the evolution of bile salt synthesis and possible therapy for infant bili

250 Bile salt synthesis is a specialized liver function in v

251 nd cytochrome P450 7a1, the key regulator of bile salt synthesis, indicating that elevated serum bile

252 limiting enzyme for the classical pathway of bile salt synthesis.

253 cascade that provides feedback inhibition of bile salt synthesis.

254 se (CYP7A1), a key enzyme for the control of bile salt synthesis.

255 al pathogen Vibrio cholerae by degrading the bile salt taurocholate that activates the expression of

256 mature biofilms to physiologic levels of the bile salt taurocholate, a host signal for the virulence

257 owever, when insulin was co-infused with the bile salt taurocholate, this was followed by a marked hy

258 One of these was revealed to be the bile salt taurocholate.

259 X bound to 7alpha-hydroxycholesterol and the bile salt tauroursodeoxycholate (TUDCA), showing how the

260 upon infusion with increasing amounts of the bile salt tauroursodeoxycholic acid, Abcg5 became fully

261 a higher critical micelle concentration for bile salts than for SDS.

262 ompany with hepatic hyposecretion of biliary bile salts, thereby inducing cholesterol-supersaturated

263 iota modify bile is through deconjugation of bile salts through bile salt hydrolase (BSH) enzymatic a

264 . flexneri forms biofilms in the presence of bile salts, through an unknown mechanism.

265 uctal fibrosis, and sensitivity toward human bile salt toxicity.

266 NA-sequencing analysis verified an important bile salt transcriptional profile in S. flexneri 2457T,

267 he established cell line displayed vectorial bile salt transport and specific phosphatidylcholine sec

268 asolateral membrane localization of multiple bile salt transport proteins in central hepatocytes and

269 dent retrieval of sinusoidal and canalicular bile salt transport systems from the corresponding membr

270 tance protein 3, and apical sodium-dependent bile salt transporter.

271 loss, and expression of major hepatocellular bile salt transporters and cytochrome P450 7a1, the key

272 tion of orthologs of known organic anion and bile salt transporters in the kidney, with lesser effect

273 estine of anaesthetised rats by means of the bile salt transporters of the ileum.

274 holyl-insulin had been taken up by the ileal bile salt transporters.

275 disulfide stress conditions are sensitive to bile salt treatment.

276 Bile salts trigger recruitment of the first hydrophobic

277 Amino acids, primary bile salts, trimethylamine and cadaverine were elevated

278 n ileum-derived metabolic hormone induced by bile salts upon gallbladder emptying after enteral nutri

279 tal bile salt load this mechanism may adjust bile salt uptake along the acinus and protect periportal

280 Instead, NTCP inhibition shifts hepatic bile salt uptake from mainly periportal hepatocytes towa

281 cotransporting polypeptide (Ntcp), the major bile salt uptake system at the sinusoidal membrane of he

282 sis demonstrated near absence of basolateral bile salt uptake transporters OATP1B2, OATP1A1, OATP1A4,

283 Net bile salt uptake was investigated in perfused rat liver

284 Disrupting hepatic bile salt uptake, by inhibition of sodium-taurocholate c

285 NTCP inhibition shifts bile salt uptake, which is generally more periportally r

286 onditions, such as in the presence of serum, bile salts, urine, and collagen and at 46 degrees C.

287 ndant and very closely related physiological bile salts, vary substantially in their destabilizing ef

288 < 0.0001), and the ratio of phospholipids to bile salt was greater (6.8 +/- 1.3 vs. 3.2 +/- 1.6, P =

289 nce, exposure of the canalicular membrane to bile salts was increased, allowing for more cholesterol

290 ndicated that hepatic uptake of unconjugated bile salts was strongly impaired whereas uptake of conju

291 rongly impaired whereas uptake of conjugated bile salts was unaffected.

292 ntial digestion processes using low and high bile salts was ~ 70% and ~ 90%, respectively.

293 Plasma total bile salts were 10-fold increased and were mostly presen

294 Luminal pH and bile salts were determined in duodenal aspirates.

295 Bile salts were rarely detected.

296 Bile salts were undetectable, using spectrophotometry an

297 tromyzonol sulfate (PZS) was the predominant bile salt, whereas the major bile salts in adult liver w

298 Here we show that mnhF confers resistance to bile salts, which can be abrogated by efflux pump inhibi

299 s multiple mechanisms to survive exposure to bile salts, which may have important implications for mu

300 nter in the gut is the high concentration of bile salts, which not only aid in food absorption but al

301 C NMR titration and negative controls with a bile salt with no secondary binding site (glycocholate)